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肥胖症和 2 型糖尿病中脑葡萄糖过度暴露和急性代谢灵活性缺乏:Zucker 和 ZDF 大鼠的 PET-[18F]FDG 研究。

Brain glucose overexposure and lack of acute metabolic flexibility in obesity and type 2 diabetes: a PET-[18F]FDG study in Zucker and ZDF rats.

机构信息

Institute of Clinical Physiology, National Research Council (CNR), Pisa, Italy.

出版信息

J Cereb Blood Flow Metab. 2010 May;30(5):895-9. doi: 10.1038/jcbfm.2010.27. Epub 2010 Feb 24.

DOI:10.1038/jcbfm.2010.27
PMID:20179723
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2949188/
Abstract

Brain glucose exposure may complicate diabetes and obesity. We used positron emission tomography with (18)F-fluorodeoxyglucose in Zucker obese, diabetic, and control rats to determine the contributions of blood glucose mass action versus local mechanisms in regulating central glucose disposal in fasted and acutely glucose-stimulated states, and their adaptations in obesity and diabetes. Our study data indicate that brain glucose uptake is dependent on both local and mass action components, and is stimulated by acute glucose intake in healthy rats. In diseased animals, the organ was chronically overexposed to glucose, due to high fasting glucose uptake, almost abolishing the physiologic response to glucose loading.

摘要

脑葡萄糖暴露可能会使糖尿病和肥胖复杂化。我们使用正电子发射断层扫描(18)F-氟代脱氧葡萄糖在 Zucker 肥胖、糖尿病和对照大鼠中,以确定血糖质量作用与局部机制在调节空腹和急性葡萄糖刺激状态下中枢葡萄糖处置中的贡献,以及它们在肥胖和糖尿病中的适应性。我们的研究数据表明,脑葡萄糖摄取既依赖于局部和质量作用成分,也受到健康大鼠急性葡萄糖摄入的刺激。在患病动物中,由于高空腹葡萄糖摄取,器官长期暴露于高葡萄糖下,几乎使葡萄糖负荷的生理反应消失。

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Acute hyperglycemia compromises cerebral blood flow following cortical spreading depression in rats monitored by laser speckle imaging.在通过激光散斑成像监测的大鼠中,急性高血糖会在皮质扩散性抑制后损害脑血流量。
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